Endothelial AT₁ and AT₂ pathways in aortic responses to angiotensin II after stress and ethanol consumption in rats

Figures & data

Figure 1. Evolution of caudal systolic blood pressure of adult male rats submitted to chronic ethanol consumption and exposed to stress, alone and in combination. Control – received water ad libitum; stress – restraint 1 h/day 5 d/week for 6 weeks; ethanol – 20% ethanol solution instead of tap water for 6 weeks; ethanol/stress – restraint stress and 20% ethanol solution for 6 weeks. “Basal” – the adaptation period for ethanol intake. Values are means ± SEM. The two-way ANOVA followed by Tukey’s post-test. (*) p < 0.05 relative to control. The number of rats per group = 8–10.

Table 1. Maximum response and EC50 values to angiotensin II in the absence and presence of losartan or PD123-319 obtained in thoracic aorta rings, with and without endothelium, isolated from adult male rats submitted or not to ethanol consumption and restraint stress, alone and in combination.

	Maximum response* (g of tension)		EC50† (×10^−8M)
Groups	With endothelium	Without endothelium	With endothelium	Without endothelium
Absence of blocker
Control	0.17 ± 0.02^A	0.68 ± 0.07^B	0.10 ± 0.02^A	0.16 ± 0.02^A
Ethanol	0.20 ± 0.04^A	0.57 ± 0.07^B	0.18 ± 0.03^A	0.31 ± 0.02^A
Stress	0.25 ± 0.03^A	0.74 ± 0.07^B	0.11 ± 0.02^A	0.22 ± 0.02^A
Ethanol/stress	0.20 ± 0.04^A	0.50 ± 0.08^B	0.10 ± 0.01^A	0.15 ± 0.02^A
Losartan presence
Control	0.07 ± 0.01^C	0.60 ± 0.09^B	6.17 ± 0.26^B	9.44 ± 0.16^B
Ethanol	0.08 ± 0.01^C	0.56 ± 0.11^B	5.37 ± 0.37^B	6.84 ± 0.20^B
Stress	0.22 ± 0.06^A	0.66 ± 0.15^B	11.9 ± 2.74^B	17.52 ± 2.68^B
Ethanol/stress	0.20 ± 0.11^A	0.55 ± 0.08^B	19.3 ± 2.65^B	8.21 ± 0.21^B
PD123-319 presence
Control	0.24 ± 0.06^A	0.79 ± 0.08^B	2.04 ± 1.14^A	0.44 ± 0.02^A
Ethanol	0.09 ± 0.02^C	0.68 ± 0.07^B	0.12 ± 0.05^A	0.33 ± 0.02^A
Stress	0.18 ± 0.05^A	0.84 ± 0.13^B	0.45 ± 0.05^A	0.42 ± 0.02^A
Ethanol/stress	0.08 ± 0.01^C	0.66 ± 0.09^B	0.20 ± 0.04^A	0.42 ± 0.02^A

EC50 – effective concentration 50%. Losartan (10⁻⁷M) – AT₁ receptor blocker; PD123-319 (10⁻⁷M) – AT₂ receptor blocker; control – received water ad libitum; stress – restraint in a metallic tube 1 h/d 5 d/week for 6 weeks; ethanol – received a 20% ethanol solution instead of tap water for 6 weeks; ethanol/stress – submitted to restraint stress and received a 20% ethanol solution for 6 weeks; inside the same parameter, i.e. maximum response and EC50, mean values sharing a common letter (A, B, or C) were not statistically different (p > 0.05, the two-way ANOVA followed by Tukey’s post-test); the number of rats per group = 8–10.

*Values are means ± SEM.

†Values are means ± SD.

Table 2. Maximum response and EC50 to angiotensin II values in the presence of indomethacin or L-NAME obtained in intact aorta rings isolated from adult male rats submitted or not to ethanol consumption and restraint stress, alone and in combination.

	Maximum response* (g of tension)		EC50† (×10^−8M)
Groups	Indomethacin	L-NAME	Indomethacin	L-NAME
Control	0.34 ± 0.04	0.47 ± 0.05	0.16 ± 0.02	0.19 ± 0.02
Ethanol	0.26 ± 0.06	0.47 ± 0.07	0.22 ± 0.03	0.12 ± 0.02
Stress	0.33 ± 0.06	0.56 ± 0.09	0.15 ± 0.02	0.11 ± 0.02
Ethanol/stress	0.24 ± 0.03	0.48 ± 0.08	0.17 ± 0.02	0.20 ± 0.02

EC50 – effective concentration 50%. Indomethacin (10⁻⁵M) – cyclooxygenase inhibitor; L-NAME (10⁻⁴ M) – nitric oxide synthase inhibitor; control – received water ad libitum; stress – restraint in a metallic tube 1 h/d 5 d/week for 6 weeks; ethanol – received a 20% ethanol solution instead of tap water for 6 weeks; ethanol/stress – submitted to restraint stress and received a 20% ethanol solution for 6 weeks; the two-way ANOVA (p > 0.05); the number of rats per group = 8–10.

*Values are means ± SEM.

†Values are means ± SD.